OSTEOPOROSIS OSTEOMALACIA RICKETS by mikesanye

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									OSTEO-
POROSIS
OSTEO-
POROSIS
Dr.Abdullah Al-Omran
   NOTE : THIS PRESENTATION DOES NOT
        REPLACE ATTENDANCE OR
       INFORMATION GIVEN IN THE
       LECTURE.IT IS INTENDED AS A
        HIGHLIGHT FOR THE TOPIC
                    OSTEOPOROSIS

OSTEOPOROSIS

DEFINITION
WHO Definition 1994:
A skeletal disease characterized by low bone mass and
   deterioration of the microarchitecture of bone tissue with a
   consequent increase in bone fragility and susceptibility to
   low trauma fractures.
Why? Imbalance between osteoblast & osteoclast function
OSTEOPOROSIS
                   OSTEOPOROSIS

OSTEOPOROSIS

INCIDENCE: 1 in 3 women and 1 in 12 men.
TYPES :
I.   (postmenoposal): thin trabicular bone
                      55-75y
                      f:m 6:1
II.  Senile       : thin both trabicular & cortical bone
                   70-85 y
                          2:1
                         OSTEOPOROSIS

RISK FACTORS + CAUSES :!
I.POST MENOPOSAL & SENILE (primary)
 -sessation of estrogen or androgen
 - bad nutritional habits during productive years (15-45yr)
   (low calcium content food , smoking,alcohol,soda drinks.
 - genetics (inheritance) & race (cocasian female)

II.Secondary :
1.medications: steroids,chronic heparin use,anticonvusants,chemotherapy.
2.immobilisation
3. Medical conditions: Anorexia Nervosa, RA, Early
   menopause,Hyperthyroidism, hyperparathyroidism, hypogonadism
   Transplantation, Cushings disease/syndrome, Chronic kidney, lung or GI
   diseases
              OSTEOPOROSIS

Clinically:
P?
P?
OSTEOPOROSIS
                  OSTEOPOROSIS

INVESTIGATIONS
1. History for risk factors
2. Physical examination
3. X-ray of lumbar and thoracic spine.
   Although >30 % of bone loss required to be visible on X-ray,
   there may be some asymptomatic wedge #s
4. Bone mineral Density measurement
5. Blood tests, FBC, ESR, serum biochemistry
6. Testosterone and Gonadotrophin levels in men
                   OSTEOPOROSIS

The Gold standard test in clinical practice is measurement of
    Bone Mineral Density (g/cm3), of the vertebral spine and
    the hip. This is as recommended by the National
    Osteoporosis society. Only vertebral measurements can be
    used to assess effectiveness of treatment at present.
1.  DEXA scans
2.  Radiographic Absorptiometry
3.  Single Photon X-ray absorptiometry (SPA)
4.  Quantitative Computer tomography
5.  Quantitative Ultrasound
OSTEOPOROSIS
              OSTEOPOROSIS

PREVENTATIVE MEASURES
Aims- to achieve an adequate peak bone mass, by ?
                 OSTEOPOROSIS

TREATMENT OF ESTABLISHED OSTEOPOROSIS:
CALCIUM + VIT. D SUPPLEMENTS

Minimum daily intake of calcium should be achieved.
  Should only be prescribed if this is not achieved by diet.
Vit D in all elderly institutionalized osteoporotics is
  recommended.

RDA Calcium = 1400 mg
RDA Vit. D = 600-800 IU.
                   OSTEOPOROSIS
HRT (OESTROGEN):
Prevent osteoporosis and slows or reverses progression.
Given at doses equivalent to 0.625mg of Premarin, it will
   increase bone density by 2% per year.
Given for 5-10 years almost halves the risk of fractures.
Has a role in corticosteroid induced osteoporosis

Contraindications: Endometrial carcinoma, Breast cancer,
  undiagnosed vaginal bleeding.
Other benefits: loss of menopausal symptoms, cardiovascular
  protection.



biphos
                     OSTEOPOROSIS
BISPHOSPHONATES:
Synthetic analogues of inorganic pyrophosphate. Inhibit bone
   resorption by osteoclasts
Alendronate (Fosamax)
    Reduces the incidence of hip, wrist and vertebral fractures in
      postmenopausal women (statistically significant)
    Contraindications-Abnormalities of oesophagus, renal problems
    Dose -10mg daily at least 30 mins before breakfast and sit
      upright for at least 30 mins
Disodium Etidronate (Didronel)
    Etidronate is effective in reducing vertebral fracture (statistically
      significant). Dose- disodium etidronate 400mg once daily.
                   OSTEOPOROSIS
OESTROGEN RECEPTOR MODULATORS (Raloxifene)
Work like oestrogen at bone without other harmful effects.
Can increase post menopausal symptoms so not to be given
  within 5 years of menopause
CALCITONIN
Non sex, non steroid hormone
Reduces resorption of bone
Nasal form at dosages of 200 units per day
Can be used for analgesia
CALCITRIOL (1,25 DIHYDROXYCHOLECALCIFEROL)
The active metabolite of vit D. 0.25 microg o.d. may reduce risk
  of vertebral #. Need monitoring of plasma calcium
                   RICKETS &
                 OSTEOMALACIA


Def.: reduction in bone mineralization !
        OSTEOMALACIA,RICKETS
Normal bone metabolism
 CALCIUM
  99% in bone.
  Main functions- muscle /nerve function, clotting.
  Plasma calcium- 50% free, 50% bound to albumin.
 Dietary needs-
  Kids- 600mg/day,
  Adolesc.-1300mg/day,
  Adult-750mg/day,
  Pregnancy-1500mg/day,
  Breastfeeding-2g/day,
  Fractures- 1500mg/day
 Absorbed in duodenum (active transport) and jejunum
  (diffusion), 98% reabsorbed in kidney prox. tubule, may be
  excreted in stool.
         OSTEOMALACIA,RICKETS
Normal bone metabolism

   PHOSPHATE
    85% in bone.
    Functions-metabolite and buffer in enzyme systems.
   Plasma phosphate mainly unbound.
    Daily requ. 1-1.5g/day
        OSTEOMALACIA,RICKETS
Regulation of Calcium & Phosphate Metabolism:
Peak bone mass at 16-25 years.
Bone loss 0.3- 0.5% per year (2-3% per year after 6th decade).
1.  Parathyroid Hormone (PTH)
2.  Vitamin D3
3.  Calcitonin
4.  Other Hormones:
    Estrogen: Prevents bone loss
    Corticosteroids: Increases bone loss
    Thyroid hormones: Leads to osteoporosis
    Growth hormones: Cause positive calcium balance
    Growth factors
          RICKETS, OSTEOMALACIA


PATHOLOGY:
          Sufficient osteoid, poor mineralization
(Rickets is found only in children prior to the closure of the
  growth plates, while OSTEOMALACIA occurs in persons of
  any age. Any child with rickets also has osteomalacia, while
  the reverse is not necessarily true).
             RICKETS, OSTEOMALACIA

CAUSES:
1.      Nutritional deficiency
     1.    Vit D
     2.    chelators of calcium- phytates, oxalates, phosphorous
     3.    Antacid abuse, causing reduced dietary phosphate binding
2.      GI Absorption defects
     1.    Post gastrectomy
     2.    Biliary disease (reduced absorption of Vitamins )
     3.    Small bowel disease
     4.    liver disease
3.      Renal tubular defects
4.      Renal osteodystrophy
5.      Miscellaneous causes
           RICKETS, OSTEOMALACIA

CLINICAL FEATURES:
 Rickets -
  Tetany , convulsions, failure to thrive,
  restlessness, muscular flaccidity.
  Flattening of skull (craniotabes),
  Thickening of wrists from epiphyseal overgrowth,
  Stunted growth,
  Rickety rosary, spinal curvature,
  Coxa vara, bowing, # of long bones

   Osteomalacia, - Aches and pains, muscle weakness loss of
    height, stress #s.
         RICKETS, OSTEOMALACIA

XRAY FINDINGS:

RICKETS
  Thickening and widening of
  physes,
  Cupping of metaphysis,
  Wide metaphysis,
  Bowing of diaphysis,
  Blurred trabeculae.
          RICKETS, OSTEOMALACIA

XRAY FINDINGS:

OSTEOMALACIA
Loosers zones - incomplete
  stress # with healing lacking
  calcium, on compression
  side of long bones.
Codfish vertebrae due to
  pressure of discs
Trefoil pelvis, due to
  indentation of acetabulae
  stress #s
          RICKETS, OSTEOMALACIA

INVESTIGATIONS:

BLOOD TESTS
  Calcium Reduced,
  Phosphate reduced
  Alkalline Phosphatase increased
  Urinary excretion of calcium diminished

Calcium phosphate products (= serum [Ca] x serum [PO4])
  normally 30. In rickets and osteomalacia is less than 24
          RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Nutritional
  Vitamin D deficiency
  Dietary chelators of calcium
        Phytates
        Oxalates
  Phosphorus deficiency (unusual)
        Antacid abuse
 Treatment- vitamin D (5000u) and Calcium (3g/day)
          RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Gastro-intestinal absorption defects
  Post-gastrectomy
  Biliary disease
  Enteric absorption defects
      Short bowel syndrome
      Rapid onset (gluten-sensitive enteropathy)
  Inflammatory bowel disease
      Crohns
      Celiac
         RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause
Renal tubular defects
  Vitamin D dependant
      type I
      type II
       Treatment; High levels of vit D

  Vitamin D resistant (familial hypophosphatemic rickets)
       Treatment; Phosphate 1-3 gm daily, Vit D3 high dose
  Fanconi syndrome I, II, III
  Renal tubular acidosis
          RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Renal Osteodystrophy – in chronic renal failure
Miscellaneous
  Hypophosphatasia
  Anticonvulsant therapy

SURGERY
For deformities

								
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